Sounds like a great kick starter from what I'm reading about alpha 1. Just finished a sdrol cycle 5 weeks ago, so it'll be a while before I cycle again, but I was gonna go with test e, 500mg/wk for 10 weeks, and use sdrol to kick start, maybe replace it with this. Sounds fun.

Sounds like a great kick starter from what I'm reading about alpha 1. Just finished a sdrol cycle 5 weeks ago, so it'll be a while before I cycle again, but I was gonna go with test e, 500mg/wk for 10 weeks, and use sdrol to kick start, maybe replace it with this. Sounds fun.

I gotcha but then running it 2 weeks into pct isn't that when you should normally start your AI in pct? What would the protocol be for your AI in pct be then?

The AI normally started 2 weeks into PCT is used to prevent estrogen rebound. With this compound that shouldn't be a problem since it aromatizes and estrogen(s) are present the whole time. That's my logic speaking again, if I'm wrong, someone please correct me.

I gotcha but then running it 2 weeks into pct isn't that when you should normally start your AI in pct? What would the protocol be for your AI in pct be then?

idk dude. im not a pro at alpha one, im just going by what ive read so far. i suppose you could switch to a non steroidal ai like erase at that point, or maybe even come off completely and let your estrogen recover since the formestane would be crushing it since the start of the cycle

The AI normally started 2 weeks into PCT is used to prevent estrogen rebound. With this compound that shouldn't be a problem since it aromatizes and estrogen(s) are present the whole time. That's my logic speaking again, if I'm wrong, someone please correct me.

this compound does not aromatize. diol's are incapable of aromatization, as well as 5a reduced androgens.

People familiar with the use of anabolic steroids know that water retention and hypertension (high blood pressure) are potential side effects. This is due to the fact that all androgenic hormones have the capacity to cause some sodium retention (and hence water retention) through direct action via androgen receptors in the kidneys. Furthermore, anabolic steroids that are estrogenic or can convert to estrogens can cause even more sodium retention via additional interaction with renal (kidney) estrogen receptors. So it’s often thought that an anabolic steroids propensity for water retention is related to its potency both as an androgen and as an estrogen (manifested via aromatization to estrogenic metabolites).
Confusion has often arisen however when people have noticed that some steroids – which traditional thinking tells us should not result in extraordinary water retention – end up doing just that. Steroids that should not aromatize to estrogens such as oxymetholone (anadrol) and methyl-1-testosterone {Alpha one is Methyl 1-androstenediol) are known to result in extreme water retention in some individuals. A recent paper* suggests a heretofore unmentioned explanation for this.
There is an enzyme that is localized primarily in the kidneys whose function is to protect the kidneys from circulating cortisol. The kidneys have receptors called mineralcorticoid receptors (MR’s) which are meant to bind to specific adrenal hormones (called mineralcorticoids) in the body such as aldosterone. The result of this binding is a signal to increase sodium and water retention in the body, while stimulating the excretion of potassium. This is an important mechanism to maintain fluid and electrolyte balance in the body.
A problem exists though in that cortisol can also bind activate these receptors. Cortisol is a widely circulating hormone and serves a multitude of functions throughout the body. However its intended biological functions do not include mineralcorticoid action in the kidneys, so to prevent this from happening the kidneys are rich in the enzyme 11b-hydroxysteroid dehydrogenase 2 (11b-HSD2). This enzyme deactivates cortisol by converting it into cortisone before it can bind to the renal MRs.
Certain substances can block 11b-HSD2, and that can lead to problems. One example is a constituent of black licorice known as glycyrrhetinic acid. This enzyme inhibition potential is precisely why people that consume a lot of black licorice are known to retain water and experience high blood pressure and electrolyte disturbances. Interestingly, legend has it that Genghis Khan had his armies ingest licorice while on the march to prevent thirst and dehydration. Of course Genghis Khan had no idea that 11b-HSD2 inhibition was responsible for these effects, and today many have been similarly unaware that this property might be responsible for some of the salt/water effects of anabolic steroids.
The study I referred to earlier found that many anabolic steroids indeed do share the ability to block this enzyme, and some of them are as powerful as glycyrrhetinic acid. Fluoxymesterone (halotestin) in particular was shown to be about as potent as glycyrrhetinic acid in this regard. This makes sense, since fluoxymesterone shares the same 11b-OH group as cortisol and can be oxidatively metabolized by 11b-HSD2 in an analogous manner.
The fact that fluoxymesterone serves as a substrate for 11b-HSD2 in this manner makes it a competitive inhibitor of the enzyme. Other anabolic steroids were also found to be potent inhibitors of the enzyme as well, although the mechanisms for these are not clear as they do not share the 11b-OH group.
In addition to fluoxymesterone other 11b-HSD2 inhibitor steroids of interest are oxymetholone (anadrol), oxymesterone, and testosterone. The question arises as to how relevant this enzyme inhibiton is in the real world. Fluoxymesterone is generally not associated excess water retention, but then again doses used are relatively low (20mg or less per day). In contrast, oxymetholone is well associated with excess water retention and the doses used of that are often high (50-150mg per day). So this may be a dose related phenomenon. Another question that I have is what sort of inhibition might methyl-1-testosterone have, since it seems to be the worst water retaining and hypertensive steroid ever made. Few have had decent explanations for this and perhaps 11b-HSD2 inhibition is a culprit (the study did not test this steroid).
A final point of interest to mention here is the intriguing fact that 11-ketofluoxymesterone (the metabolite formed in the kidneys as mentioned previously) is actually a stronger anabolic steroid than fluoxymesterone according to animal tests. I find that interesting because one would also expect it to generally lack the troublesome enzyme inhibition that can lead to mineralcorticoid related disturbances. Maybe if the inventors of fluoxymesterone had decided to just simply oxidize the 11b-OH group they would have ended up with a more healthy and effective steroid to sell.
*http://www.ncbi.nlm.nih.gov/pubmed/22273746